METHODS: Twenty-nine children in each group, matched for age, sex and ethnicity, were assessed using the Glasgow outcome Scale (GOS), Weschler Intelligence Scale for Children (WISC-III), Movement Assessment Battery for Children (Movement ABC), Wide Range Assessment of Learning and Memory (WRAML) and a standardised neurological examination 6 months post-injury. Parental reporting of pre- and post-injury behaviour was documented using the Child Behaviour Checklist (CBCL).
RESULTS: Seven (24.1%) children with sCHI and three (10.3%) orthopaedic controls had residual motor deficits. Three (10.3%) children with sCHI and none in the other groups faced problems with independent ambulation. Twenty-seven (93.1%) of those with sCHI and all children in the other groups had GOS scores of good recovery or moderate disability. Twenty-two (81.5%) sCHI, five (18.5%) mCHI and one (3.7%) orthopaedic control reported a deterioration in school performance. MANOVAS identified a significant injury group effect for performance skills (P = 0.007), verbal skills (P = 0.002), memory and learning (P = 0.001) and motor skills (P = 0.001). Repeated measures ANOVA for pre- and post-injury CBCL scores showed significant differences related to somatic complaints (P = 0.004), problems of socialising (P = 0.003), delinquency (P = 0.004), aggressiveness (P = 0.010), thought (P < 0.001) and attention (P < 0.001). Post-hoc univariate analysis showed the significant differences were between that of the sCHI children and the other two groups.
CONCLUSION: Although most sCHI children seemed to have made good physical recovery, there were cognitive, motor, memory and learning difficulties and behavioural problems concomitant with a deterioration in school performance compared with those with lesser or no head injury. This highlights the need for better integrated rehabilitation services to enable a gradual return into mainstream school.
METHODS: Male Sprague Dawley rats were subjected to permanent bilateral occlusion of common carotid arteries (PBOCCA) or sham surgery. Then, PBOCCA rats received ip injections with, either vehicle (control group), the muscarinic receptor agonist oxotremorine (0.1 mg/kg), or the acetylcholinesterase inhibitor physostigmine (0.1 mg/kg). Cognitive functions were evaluated using a passive avoidance task and the Morris water maze test. In addition, hippocampal LTP was recorded in vivo under anaesthesia.
RESULTS: The PBOCCA rats exhibited significant deficits in passive avoidance retention and spatial learning and memory tests. They also showed a suppression of LTP formation in the hippocampus. Oxotremorine and physostigmine significantly improved the learning and memory deficits as well as the suppression of LTP in PBOCCA rats.
CONCLUSIONS: The present data suggest that the cholinergic system plays an important role in CCH-induced cognitive deficits and could be an effective therapeutic target for the treatment of VaD.
METHOD: Cognitive decline was determined by Montreal Cognitive Assessment (MoCA). Oxidative stress markers (malondialdehyde-MDA and superoxide dismutase-SOD) were determined and DNA damage was assayed using Alkaline Comet Assay. Toenail samples were taken and analyzed using ICP-MS to determine trace element levels.
RESULTS: A total of 62.1 % of subjects had cognitive impairment. Subjects with cognitive impairment had significantly higher levels of MDA and DNA damage as compared to the group with normal cognitive function; MDA (2.07 ± 0.05 nmol/L vs 1.85 ± 0.06 nmol/L) (p<0.05) and DNA damage (% Tail Density, 14.52 ± 0.32 vs 10.31 ± 0.42; Tail Moment, 1.79 ± 0.06 vs 1.28 ± 0.06) (p<0.05 for all parameters). However, the level of SOD among subjects with cognitive impairment (6.67 ± 0.33 u.e/min/mg protein) was lower than the level among those with normal cognitive functions (11.36 ± 0.65 u.e/min/mg protein) (p<0.05). Multiple logistic regression revealed the predictors for cognitive impairment among the subjects were DNA damage (Adjusted odd ratio [OR], 1.37; 95% confidence interval [CI], 1.18-1.59), level of trace elements in toenails namely, lead (OR, 2.471; CI, 1.535-3.980) and copper (OR, 1.275; CI, 1.047-1.552) (p<0.05).
CONCLUSION: High levels of lead and copper can lead to increase in oxidative stress levels and are associated with DNA damage that eventually could be associated with cognitive decline.